Project description:Whole genome sequencing of 10 HCLc tumor and matched-germline T cells. Genomic DNA from highly purified HCLc tumor and T cell populations were utilized for library preparation using NEBNext Ultra DNA library prep kit. Sequencing was performed as 150 bp paired end sequencing using four lanes of an Illumina HiSeq4000 to an average depth of 12X. Reads from each library were aligned to the human reference genome GRCh37 using BWA-MEM (v0.7.12). The analysis of somatic genetic alterations in WGS data from tumor-germline pair HCLc samples was divided based on the nature of the mutation, as follow: single-nucleotide variants (SNVs), indels, CNAs and SVs. Moreover, COSMIC mutational signatures and subclonal architecture was inferred for each tumor.
Project description:Deep RNA-Seq of two Brassica rapa genotypes—R500 (var. trilocularis, Yellow Sarson) and IMB211 (a rapid cycling variety)—using eight different tissues (root, internode, leaf, petiole, apical meristem, floral meristem, silique, and seedling) grown across three different environments (growth chamber, greenhouse and field) and under two different treatments (simulated sun and simulated shade) generated 2.3 billion high-quality Illumina reads.
Project description:Objective: To determine alterations in plasma miRNAs during early stages (2 weeks and 6 weeks) post ACL reconstruction surgery MicroRNA libraries were prepared using the QIAseq miRNA Library Kit and sequenced on the Illumina NextSeq550. MiRNA reads were then aligned with the mature miRNAs from miRBase v22.1 and human reference genome to create counts for each sample.
Project description:Poor prognosis of small cell lung cancer (SCLC) is mainly attributed to its highly metastatic capability. Here we identify the SMC and Non-SMC from Rb1L/L/Trp53 L/L mouse model through FACS with NE and mensenchymal markers. In order to identify functions of these two subpopulations during SCLC malignant progression, we compared their metastatic capability by allograft experiment. In addition, we find that the SMC is progressively transited from the Non-SCLC during mouse SCLC malignant progression. Further investigation reveals that genetic disruption of the SWI/SNF chromatin-remodeling complex, in RP model abrogates SMC phenotype maintenance and SCLC metastasis. In search of important downstream regulators, we find that TAZ, the core transcription cofactor of the Hippo pathway, is epigenetically silenced by SWI/SNF complex during this process. Collectively, our data link phenotypic transition to cancer metastasis and identify TAZ as a critical molecular switch that controls SCLC plasticity.